Pathophysiology of endotoxin shock in the primate

Abstract

The intravenous administration of coliform endotoxin to healthy baboons produced a precipitous fall in renal artery flow, a profound drop in the platelet count, and a marked increase in plasma norepinephrine levels within 3 minutes. There was no significant change in aortic pressure, central venous pressure, cardiac output, or circulation time over this period. After 3 to 10 minutes, simultaneous shortening of the plastic clotting time and intensive stimulation of the fibrinolytic system occurred. By 60 minutes, progressive deterioration of the coagulation mechanism had occurred. After the initial rise, the plasma norepinephrine levels began to fall and were near normal at 120 minutes. Response of isolated atria from baboons pretreated with endotoxin showed that endotoxin pretreatment caused reduced responsiveness to l-norepinephrine and tyramine. These studies have clarified the pathophysiology of endotoxin shock in the primate to some degree, suggesting that selective vasospasm, intravascular coagulation, and reduced myocardial response all play a part.